POS0167 THE ANTIMALARIAL PROTECTIVE EFFECT AND A CLEAR CUT-OFF POINT FOR STEROID CUMULATIVE DOSE ASSOCIATED WITH DAMAGE ACCRUAL ON A 10-YEAR FOLLOW-UP SYSTEMIC LUPUS ERYTHEMATOSUS COHORT
Authors: R. Montes, E. Klumb
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Assessing damage accrual (DA) in patients with systemic lupus erythematosus (SLE) is complex but mandatory. Damage might be caused by the disease itself, comorbidities, and/or its pharmacological treatment or both. Among the pharmacological agents used to treat SLE, glucocorticoids (GC) are arguably the main cause of damage followed by lupus flares [1,2]. <h3>Objectives</h3> This study aims to identify precise values of damage accrual related to damage in the long-term, the predictive positive and negative values for damage accrual of different steroid burden cut-offs points and the influence of other drugs, socioeconomic, ethnical and clinical aspects with damage in lupus patients. <h3>Methods</h3> A 10-years follow-up cohort of initially 190 patients, 147 alive at the end, with data regarding SLICC/ACR damage index (SDI) [3], clinical, social, economic and ethnical characteristics were recorded. SDI and medications accrual including GC were analyzed yearly both by patients interviews and chart reviews. A receiver operator characteristic (ROC) curve was developed to better comprehend relations among GC and damage, non-parametric data was analyzed by Mann-Whitney test and regression analyses was performed with Pearson test to evaluate factors related to DA over 10 years. <h3>Results</h3> Patients already with damage at baseline (SDI &gt; 0) needed lesser GC accrual to develop new damage (4.2 g x 7.0 g, <i>p</i> = 0.022). Mean annual accrual of GC over a cut-off determined by the ROC curve analyses of 3.0 g (mean 8.22 mg per day) was independently associated with damage enhancement by SDI during the 10 years follow-up period compared to less than 3.0 g per year (OR= 5.32 <i>p</i> = 0.001) on multivariate logistic analyses (MLA) using stepwise forward, patients with mean GC annual accrual above this point present a positive predictor value (PPV) for DA of 88.7 %. Other cut-off points were evaluated and even for mean annual GC accrual of 0.5 g (approximately 1.37 mg per day) patients above this lower cut-off point had a PPV for DA greater than 75 % and the negative predictive value for the ones under this point was only 45.8 %. Patients using antimalarials (AMA) showed a protective effect for developing new damage (OR= 0.12, <i>p</i> = 0.009) on MLA and presented a higher proportion of patients under the 3.0 g/year of mean annual GC accrual (<i>p</i> = 0.005). Patients with lupus nephritis (OR= 2.50, <i>p</i> = 0.030), pleuritis (OR= 4.00, <i>p</i> = 0.003), age older than 44 years (OR= 5.14, <i>p</i> = 0.003) at recruitment and the use of azathioprine during the follow-up period (OR = 2.32, <i>p</i> = 0.044) were also independently associated with damage on MLA with stepwise forward. <h3>Conclusion</h3> The present cohort study findings highlight the protective effect of AMA regarding damage and its possible relation with a lower GC burden in the long-term. The harmful effects of GC on DA measured by SDI in patients with lupus is ratified. In contrast with other studies, it is shown that even low doses of GC might be associated with DA when chronically used in the long-term and no safe GC burden was found. There might be no safe GC dose for patients with more than a decade of SLE and physicians might need to pursuit SLE treatment with zero GC dose for the long-term when disease remission is established as soon as possible. <h3>References</h3> [1]Ruiz-Arruza I, Ugarte A, Cabezas-Rodriguez I, Medina JA, Moran MA, Ruiz-Irastorza G. Glucocorticoids and irreversible damage in patients with systemic lupus erythematosus. Rheumatology (United Kingdom). 2014;53(8):1470–6. [2]<b>Thamer</b> M, Hernán MA, Zhang Y, Cotter D, Petri M. Prednisone, lupus activity, and permanent organ damage. Journal of Rheumatology. 2009;36(3):560–4. [3]<b>Gladman</b> DD, Urowitz MB, Goldsmith CH <i>et al</i>. Arthritis &amp; Rheumatism Vol. 40, No. 5, May 1997, pp 809-813 1997, American College of Rheumatology <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> RICARDO MONTES Grant/research support from: ISS program - GSK, Evandro Klumb: None declared.